STC-1

STC-1

Cat.No.: CSC-C9250W

Species: Mus musculus (Mouse)

Source: Intestine; Small Intestine; Duodenum

Morphology: epithelial-like

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Cat.No.
CSC-C9250W
Description
The STC-1 cell line was derived from the intestinal tumors of RIP1Tag2/Rip2pyST1 double transgenic mice.
Species
Mus musculus (Mouse)
Source
Intestine; Small Intestine; Duodenum
Recommended Medium
90% DMEM+ 10% h.i.FBS
Morphology
epithelial-like
Disease
Mouse Intestinal Tract Neuroendocrine Adenoma
Storage and Shipping
liquid nitrogen vapor phase
Synonyms
STC-1; STC1
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

STC-1 is a murine intestinal enteroendocrine cell line originally established in 1990 from an endocrine tumor of the small intestine in double-transgenic mice harboring rat insulin promoter-driven polyoma small T antigen and SV40 large T antigen transgenes. As one of the three most extensively characterized enteroendocrine cell models, STC-1 offers a uniquely plurihormonal secretory repertoire, producing and releasing cholecystokinin (CCK), secretin, glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), neurotensin, and proglucagon-derived peptides including GLP-1, GLP-2, and oxyntomodulin in a regulated, stimulus-dependent manner.

This broad hormonal profile closely mirrors the overlapping hormone expression patterns of native upper gastrointestinal enteroendocrine cells, making STC-1 exceptionally relevant for investigating gut-brain signaling, nutrient sensing, and metabolic regulation. The cells mount robust, dose-dependent secretory responses to diverse physiological stimuli—including monosaccharides, fatty acids, amino acids, and bioactive peptides—providing a reliable platform for high-throughput screening of food-derived bioactives, satiety modulators, and incretin secretagogues. With decades of peer-reviewed validation and standardized culture protocols, STC-1 remains the gold-standard murine model for mechanistic studies of intestinal hormone secretion and therapeutic discovery in metabolic disease.

LPS Significantly Alters α-synuclein Intensity in A TLR4-Dependent Manner in STC-1 Cells

The STC-1 cell line, which models an enteroendocrine population capable of communicating with the gut microbiota, immune and nervous systems, was treated with a TLR4 inhibitor (TAK-242) prior to microbial lipopolysaccharide (LPS) exposure to investigate the role of TLR4 signaling in α-synuclein alterations. Antibodies targeting the full-length protein (α-synuclein) and the Serine-129 phosphorylated form (pS129) were used.

Confocal microscopy revealed heterogenous distribution of α-synuclein and pS129 in STC-1 cells, with prominent pS129 staining along cytoplasmic processes. Imaging flow cytometry further quantified the relationship between various α-synuclein morphometric features. Thereafter, imaging flow cytometry demonstrated a dose-specific effect of LPS, where the low (8 μg/mL), but not high dose (32 μg/mL), significantly altered measures related to α-synuclein intensity, distribution, and localization. Pre-treatment with a TLR4 inhibitor TAK-242 alleviated some of these significant alterations. This study demonstrates that LPS-TLR4 signaling alters the intracellular localization of α-synuclein in enteroendocrine cells.

Inhibiting TLR4 prevented some LPS-induced changes to α-synuclein.
Fig. 1. Inhibiting TLR4 prevented some LPS-induced changes to α-synuclein (Gorecki, Anastazja M., et al., 2025).

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